{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T03:50:29Z","timestamp":1792036229023,"version":"4.4.0"},"reference-count":50,"publisher":"Wiley","issue":"57","license":[{"start":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T00:00:00Z","timestamp":1787270400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T00:00:00Z","timestamp":1787270400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82403844"],"award-info":[{"award-number":["82403844"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Memory T cells exhibit long\u2010term persistence, a defining feature that underpins durable clinical responses to adoptive immunotherapies. The mechanisms that integrate metabolic cues with transcriptional control of memory fate remain undetermined. Here, we identify HS1\u2010binding protein 3 (HS1BP3) is preferentially expressed in memory CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells. HS1BP3 deficiency reduced memory\u2010associated gene expression in CD8\n                    <jats:sup>+<\/jats:sup>\n                    OT\u20101 T cells following\u00a0\n                    <jats:italic>Listeria monocytogenes\u2013<\/jats:italic>\n                    ovalbumin infection and impaired antitumor responses. Loss of HS1BP3 induces metabolic reprogramming characterized by reduced oxidative phosphorylation (OXPHOS) and altered nicotinamide metabolism, accompanied by increased NAD\n                    <jats:sup>+<\/jats:sup>\n                    and nicotinamide metabolite 1\u2010methylnicotinamide (MNAM) abundance. HS1BP3 interacted with Sirtuin 1 (SIRT1), and its deficiency is associated with increased SIRT1 activity, enhanced Forkhead box O3 (FOXO3) signaling, and reduced expression of memory\u2010associated transcription factor B cell lymphoma 6 (BCL6). Moreover, accumulation of MNAM impairs the antitumor activity of CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cells. Importantly, elevated levels of HS1BP3 drive chimeric antigen receptor (CAR) \u2010T cells towards a memory phenotype and improve tumor control. Collectively, our findings identify HS1BP3 as a regulator of CD8\n                    <jats:sup>+<\/jats:sup>\n                    T cell memory and indicate that its effects are associated with alterations in nicotinamide metabolism and the SIRT1\u2013FOXO3\u2013BCL6 signaling axis. These observations support the therapeutic potential of HS1BP3\u2010engineered CAR\u2010T cells across solid tumors.\n                  <\/jats:p>","DOI":"10.1002\/advs.77284","type":"journal-article","created":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T14:13:22Z","timestamp":1787321602000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Nicotinamide Metabolism Constrains Memory CD8\n                    <sup>+<\/sup>\n                    T Cell Formation Through a Putative HS1BP3\u2010SIRT1\u2010FOXO3\u2010BCL6 Axis"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0000-2931-0131","authenticated-orcid":false,"given":"Siyang","family":"Wang","sequence":"first","affiliation":[{"name":"Biotherapy Center and Cancer Center The First Affiliated Hospital of Zhengzhou University  Zhengzhou Henan 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